Attentional bias (AB) is the excess allocation of attention toward a particular stimulus type, a phenomenon that can be readily measured in laboratory paradigms. Among people with substance use disorders (SUDs), including alcohol use disorders (AUDs), AB toward drug-related stimuli is widely reported. Such addiction AB is of clinical importance as it has been reported to correlate with drug craving, addiction severity, and treatment outcomes. Addiction AB is thought to reflect incentive sensitization processes associated with repeated pairing of sensory stimuli with the rewarding properties of reinforcing substances. Pairing non-drug rewards with simple geometric visual stimuli can also elicit AB toward these reward-paired cues (reward-driven AB) during brief laboratory conditioning. This is true for healthy young adults with no SUD history, and for methadone maintained heroin addicts, such reward-driven AB is greatly magnified. Reward-driven AB has not yet been investigated in other SUD (or at-risk) populations, and the relationship between addiction AB and reward-driven AB is unknown. Moreover, no studies to date have investigated the neural mechanisms of reward-driven AB. We hypothesize that a generalized hypersensitivity of the attention system to reward-related stimuli underlies both forms of AB. Published work from other labs, and our own preliminary data show that heavy, binge drinkers exhibit AB to alcohol cues. We predict that reward-driven AB will also be elevated in heavy, binge drinkers compared to moderate drinkers. Thus, the proposed study will first investigate the relationship between AB to alcohol cues and reward-driven AB in heavy binge drinkers versus moderate drinkers (Aim 1). In addition, we hypothesize that reward-driven AB is mediated by reward-predicting phasic dopamine (DA) release from the ventral tegmental area (VTA) projections to the nucleus accumbens (NAc), which are triggered or otherwise regulated by the prefrontal cortex (PFC). Thus, we will measure the effect of dampening phasic DA release, via an established amino acid depletion method, on reward-driven AB, comparing heavy binge-drinkers to moderate drinkers (Aim 2). Finally, as a first step toward identifying the neural circuit bases of reward-driven AB we will measure functional connectivity of the VTA with frontal and striatal regions from brief, resting-state fMRI scans collected immediately prior to behavioral testing, comparing DA depleted and control session data (Aim 3). We predict that DA depletion will reduce reward-driven AB, and that the magnitude of this behavioral change will be associated with reduced connectivity of the VTA with frontal nodes and/or increased connectivity with the NAc. This work may ultimately lead to the identification of generalized abnormalities in reward sensitivity associated with heavy, binge drinking that may increase susceptibility to, or maintain, addictive behaviors. An understanding of these neural processes is fundamental to determining how the brain enables us to attend and respond to environmental stimuli of value and may ultimately have implications for treating addictive disorders.